I. Infectious Bovine Rhinotracheitis
Bovine herpesvirus type 1 (hereinafter "BHV-1"), more commonly known as infectious bovine rhinotracheitis virus (hereinafter "IBRV"), has been associated with respiratory, reproductive, enteric, occular, central nervous system, neonatal, mammary, and dermal infections of cattle. Evidence for the association of IBRV with diseases of the respiratory tract was first obtained in the early 1950's. It has since become apparent that infectious bovine rhinotracheitis (hereinafter "IBR") has a worldwide distribution. Clinical symptoms are characterized by a sudden onset of hyperthermia, anorexia, and depression. The severe inflammation of the epithelial surfaces of the respiratory membranes often progresses to a necrotic rhinotracheitis (see: Schroeder, R.J. and Moys, M.D., J. Am. Vet. Med. Assoc. 125:471-472 (1954); McKercher, D.G., Moulton, J.E., and Jasper, D.E., Proc. U.S. Livestock Sanit. Assoc. 58:260-269 (1955); Gibbs, E.P.J. and Rweyemamu, M.M., The Vet. Bull. 47:317-343 (1977); Kahrs, R.F., J. Am. Vet. Med. Assoc. 171:1055 1066 (1977); Moorthy, A.R.S., Vet. Record 116:98 (1985); Ross, H.M., Vet. Record 113:217-218 (1983); Guy, J.S., Potgieter, L.N.D., McCracken, M., and Martin W., Am. J. Vet. Res. 45:783-785 (1984); and Engels, M., Steck, F., and Wyler, R., Arch. Virol. 67:169-174 (1981)).
In natural outbreaks of the respiratory form of the disease, conjunctivitis, manifested by a copious discharge, extensive hyperemia and edema of the conjunctiva, is also prominent. Infectious pustular vulvovaginitis and balanoposthitis are also caused by BHV-1, and are characterized by hyperemia of the vulvovaginal and preputial mucous membranes. This can lead to pustule formation and ulceration.
The spread of the disease in naturally and artificially bred cattle poses a serious problem, especially with the continued, widespread use of frozen semen. Recurrent shedding of virus from infected bulls also constitutes a significant threat to the artificial insemination industry in the United States and to the worldwide distribution of bovine germ plasm. The incrimination of BHV-1 as an etiologic agent of oophoritis and salpingitis with resultant infertility and sterility adds to the seriousness of the infection.
BHV-1 is widely recognized as a cause of abortion, stillbirths, and infertility. Most naturally occurring abortions occur between the fourth and seventh months of gestation, but cattle may abort from BHV-1 infections throughout gestation. Respiratory disease and conjunctivitis may or may not be observed prior to abortion.
Meningoencephalitis is another of the sequela to BHV-1 infection. Neurotropic symptoms are observed most often in calves under 6 months of age. The rate of encephalitis may vary from an occasional animal to a large portion of the herd.
BHV-1 infections of species other than cattle have been described (see: Fulton, R.W., Downing, M.M, and Hagstad, H.V., Am. J. Vet. Res. 43:1454-1457 (1982) and Lupton, H.W., Barnes, H.J., and Reed, D.E., Cornell Vet. 70:77-95 (1980)). Natural infections occur in swine, goats, water buffalo, wildebeests, ferrets, and mink. BHV-1 has been blamed for epizootics of vaginitis and balanitis in swine, and BHV-1 has been isolated from stillborn and newborn pigs in herds with a history of reproductive problems. According to serologic studies, about 11% of swine sera from Iowa and Texas herds contain BHV-1 antibody titers. Experimental infections have been established in swine fetuses, goats, mule deer, ferrets, and rabbits (see: Joo, H.S., Dee, S.A., Molitor, T.W., and Thacker, B.J., Am. J. Vet. Med. Assoc. 45:1924 1927 (1984)).
The severity of illness resulting from BHV-1 infections depends upon the virus strain and on the age of the animal affected. After recovery from infection, animals may show clinical signs of recurrent disease without being reexposed to the virus. Recurrent disease without reexposure occurs because the virus remains dormant, i.e. latent, in neurons of the sensory ganglia of its host and can be reactivated, even after long periods (see: Homan, E.J. and Easterday, B.C., J. Infect. Dis. 146:97 (1982); Homan, E.J. and Easterday, B.C., Am. J. Vet. Res. 44:309-313 (1983); and Ackermann, M., Peterhans, E., and Wyler, R., Am. J. Vet. Res. 43:36-40 (1982)). Dexamethasone treatment can also provoke nasal shedding of the virus with or without clinical symptoms of active IBR. This suggests that reactivation and release from neuronal sites and, possibly, persistent infection of other tissues can occur (see: Rossi, C.R., Kiesel, G.K., and Rumph, P.F., Am. J. Vet. Res. 43:1440-1442 (1982)).